Beta2 integrin/ICAM expression in Crohn's disease.
We have previously reported on the expression of the beta2 integrin family of adhesion molecules and their ligands, the ICAM molecules, in the normal human intestine. These molecules likely have a role to play in the inflammatory response and, therefore, were studied in a group of patients with Crohn's disease. A comprehensive study was undertaken in both colon (n = 8) and ileum (n = 10) specimens from 15 patients who underwent surgical resections. Immunohistochemistry was performed for CD18, CD11a, CD11b, CD11c, alphad, ICAM-1, ICAM-2, and ICAM-3. Each of the mucosal, submucosal, muscle, and adventitial layers were scored for expression. Specimens from normal colon (n = 15), normal ileum (n = 6), and ulcerative colitis (n = 7) were used for comparisons. Compared with normal, the expression in the colon mucosa and submucosa in Crohn's disease was increased for all beta2 integrins. Mucosal CD11c expression was significantly greater in Crohn's disease than in ulcerative colitis. In the colon muscle and adventitial layers the expression in Crohn's disease was similar to normal but increased compared with ulcerative colitis. In Crohn's disease ileum, the beta2 integrin mucosal and submucosal expression was similar to normal; however, muscle and adventitial expression was increased, particularly for CD11c. Colon ICAM-1, ICAM-2, and ICAM-3 expression in Crohn's disease was similar to that seen in ulcerative colitis. ICAM-1 was predominantly expressed on endothelium but in the inflammatory bowel diseases was also evident on mucosal mononuclear cells. ICAM-1 and ICAM-2 expression was increased in Crohn's disease colon and ileum compared with normals. This was most notable in ileal mucosa since ICAM-2 is typically absent in normal ileal mucosa. In summary, we are reporting a comprehensive immunohistochemical study of the differential expression of beta2 integrins, including the newly described alphad molecule, and the ICAM molecules in all layers of the colon and ileum from patients with Crohn's disease. The increased expression of these molecules may have implications for therapeutic interventions in Crohn's disease.
Bernstein
C N
CN
Department of Medicine, University of Manitoba, Winnipeg, Manitoba, R3A 1R9, Canada.
Sargent
M
M
Gallatin
W M
WM
D015703:Antigens, CD / Q000096:biosynthesis; D018821:CD18 Antigens / Q000096:biosynthesis*; D015815:Cell Adhesion Molecules / Q000096:biosynthesis*; D003093:Colitis, Ulcerative / Q000378:metabolism / Q000473:pathology; D003106:Colon / Q000378:metabolism; D003424:Crohn Disease / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007082:Ileum / Q000378:metabolism / Q000473:pathology; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D007421:Intestine, Small / Q000378:metabolism / Q000473:pathology
D015703:Antigens, CD; D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; C065289:ICAM2 protein, human; D018799:Intercellular Adhesion Molecule-1